tbuckley/cabot-search huggingface dataset:
Abstracts From the 46th Annual Conference on Cardiovascular Disease Epidemiology and Prevention
Journal: Circulation (2006)

High white matter grade (WMG) on brain cranial magnetic resonance imaging (MRI) is associated with elevated systolic blood pressure (SBP) and other measures of clinical and subclinical cardiovascular disease (CVD), and is a risk factor for clinical stroke, dementia, and declining physical functioning.High WMG is likely due to small vessel disease, which may contribute to loss of brain tissue with ventricular enlargement and high ventricular grade (VG) on MRI.In the Cardiovascular Health Study (CHS), we evaluated the relationship of WMG and VG, measured on a scale from 0 (no WM hyperintensity) to 9 (most severe) in 1992-94, to total and cause-specific mortality through June 30, 2002 among 3,240 women and men, mean age 75.We tested the hypothesis that higher WMG and VG were related to risk of total and CVD mortality after adjustment for other key risk factors.All-cause, CVD, and non-CVD death rates increased with increasing WMG and VG grades.For example, for women aged 65-74, the all-cause death rate was 16.6 per 1,000 person-years for WMG Ͻ 2 compared to 54.4 for WMG Ͼ6.The association remained after adjustment for CVD risk factors.The higher mortality for increasing WMG and VG persisted over the 12-year follow up.Risk associated with WMG or VG did not differ by sex, race or age (p interactions all Ͼ0.05).Participants who were below the median for both WMG and VG had a hazards ratio of 0.61 (0.43-0.87) of death compared to participants at or above the median on both measures.At age 75, the average survival of participants with WMG and VG below the median and without subclinical CVD was 18.7 years, to approximately age 93, compared to 11.5 years for those with WMG and VG at or above the median and with subclinical disease.These variables may have the strongest associations of any variable with longevity among older individuals.High WMG and VG on MRI are strongly associated with mortality in older persons, possibly reflecting the effects of small vessel disease in the brain.
Controversy continues as experts ponder zidovudine's role in early HIV infection
Authors: P. Cotton
Journal: JAMA (1990)

SCIENTISTS are not unanimous in endorsing zidovudine (azidothymidine [AZT]; Retrovir [Burroughs Wellcome Co]) therapy for patients infected with the human immunodeficiency virus (HIV) whose CD4 cell counts are above 200/mm<sup>3</sup>. Doubts are most notable among investigators at the Veterans Administration (VA) and in Europe who have not seen benefit in such patients in their own ongoing trials with the only approved drug that fights the retrovirus thought to cause acquired immunodeficiency syndrome (AIDS). The Food and Drug Administration (FDA) on March 2 extended label indications for zidovudine, raising the CD4 cell count threshhold for therapy implementation from 200 to 500. The change was based on data from two National Institute of Allergy and Infectious Diseases (NIAID) trials, dubbed numbers 016 and 019. In patients with CD4 counts between 200 and 500, low dosages (500 to 1200 mg/d) were well tolerated, significantly delayed onset of opportunistic infections but not malignancies
Massachusetts Medical Society
Authors: John Figgis Jewett
Journal: New England Journal of Medicine (1959)

SEASON'S GREETINGSAs spokesman for the Massachusetts Medical Society I take this opportunity of extending to all the Society's fellows and all the readers of the Journal a Merry Christmas and a Happy New Year!Lawrence R. Dame, M.D. President COMMITTEE ON MATERNAL WELFARE*Placenta Increta and Placenta Praevia, with Post-Partum HemorrhageA thirty-year-old gravida 3, para 2, died in the operating room during her third cesarean section. The first had been done at forty-one weeks because of cephalopelvic disproportion four years earlier, and the second a year afterward, the sole complications being swollen ankles and an "irritable heart" during . . .
A retrospective analysis on the impact of preoperative neutrophil to lymphocyte ratio in stage II colon cancer.
Authors: Deepna Deepak Jaiswal, Suparna Mantha, Luis Seija, Yolanda Munoz, Lucas Wong
Journal: Journal of Clinical Oncology (2017)

e15146 Background: Inflammation has a critical role in tumor genesis and progression of cancer. The neutrophil to lymphocyte ratio (NLR) is an indication of balance between the immune systems pro and defense mechanism against cancer. Elevated NLR is of interest in many cancers, including colon cancer. Although surgery is the mainstay of treatment for early stage colon cancer, adjuvant chemotherapy for stage II colon cancer has remained debatable. We proposed to study the impact of the NLR in patients with stage II colon cancer and to identify high risk patients who would benefit from adjuvant chemotherapy. Methods: Three hundred and eighty patients diagnosed with Stage II colon cancer at our institution were included in this retrospective study. Kaplan-Meir curves and multivariate Cox-regression analyses were calculated for overall survival. Results: Univariate analysis showed NLR was not statistically significant as predictor of mortality (p-value = 0.0857). However, after adjusting for recurrence, chemotherapy, age, white blood cell count, the NLR was predictive for survival, with a hazard ratio of 1.05 and 95% confidence interval of (1.006 - 1.1). Recurrence and age were also significant predictors of survival (p-values of &lt; 0.0001 for both), and HR of 3.1 (2.0 – 4.6) and 1.4 (1.2 – 1.5), respectively. Conclusions: The neutrophil to lymphocyte ratio might be an independent prognostic marker for overall survival in stage II colon cancer patients. Given the retrospective nature of our study, further studies are indicated to confirm our findings.
Cardiac Asthma
Authors: THOMAS A. LOMBARDO, TINSLEY R. HARRISON
Journal: Circulation (1951)

Cardiac asthma may be defined as the clinical syndrome induced by acute passive congestion and edema of the lungs. It occurs when the left side of the heart suffers from a sudden disproportion between work load and work capacity. It may result, therefore: (1) from disorders which cause rapid impairment of the myocardium, the load being constant (for example, myocardial infarction); (2) from disorders which suddenly increase the resistance or pressure load (such as paroxysmal hypertension consequent to an adrenal medullary tumor); (3) from disorders which markedly elevate the inflow or venous load without impairing the myocardium (such as strenuous exertion in a person with mitral stenosis); or (4) from a combination of these factors. The most common cause is increased venous return in a recumbent subject with left ventricular strain consequent to hypertension. Of the numerous conditions which may produce increased venous return, nocturnal reabsorption of extracellular fluid from dependent parts is probably the most common. The therapeutic implications are obvious. Cardiac asthma must be differentiated from the various primary diseases of the lungs which cause paroxysms of wheezing or panting. The differentiation is usually readily made by simple clinical measures; in doubtful instances measurements of circulation time may be of crucial value. The management of cardiac asthma involves chiefly three therapeutic principles: (1) Control of precipitating factors (and especially treatment of latent edema and control of nocturnal cough); (2) measures aimed at reducing the inflow load (sitting position, morphine, venesection, tourniquets on extremities, positive pressure breathing); (3) attempts to reduce the amount of residual blood in the left ventricle (rapid digitalization, use of oxygen, and aminophyllin). A severe attack of cardiac asthma associated with rapidly developing pulmonary edema constitutes one of the commonest and gravest of all medical emergencies. There are few conditions in the broad domain of internal medicine in which prompt and energetic therapy, based on an understanding of the mechanism of the disorder, can produce such immediate and gratifying benefit.
&lt;emph&gt;Medicolegal&lt;/emph&gt;
Journal: JAMA (2009)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Book Review Architectural Principles in Arthrodesis . By H. A. Brittain, M.A., M.Ch. With a foreword by Harry Platt, M.D., M.S., F.R.C.S., F.A.C.S. (hon.). 8°, cloth, 132 pp., with 144 illustrations. Baltimore: The Williams and Wilkins Company, 1942. $6.00.
Journal: New England Journal of Medicine (1943)
Woman's Auxiliary
Journal: JAMA (1971)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
New Names
Journal: JAMA (1975)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 2732: Frameshift neoantigen vaccination prevent Lynch syndrome mouse model intestinal cancer
Authors: Ozkan Gelincik, Hamza Ibrahim, Mine Ozkan, Aysel Ahadova, Shizuko Sei, Robert Shoemaker, Mattias Kloor, Magnus Von Knebel Doeberitz, Steven M. Lipkin
Journal: Cancer Research (2019)

Abstract Microsatellite-unstable (MSI) cancers occurring in the context of Lynch syndrome elicit pronounced tumor-specific immune responses directed against frameshift peptide (FSP) neoantigens, which result from mismatch repair (MMR) deficiency-induced insertion/deletion mutations in coding microsatellites (cMS). We have recently completed a clinical phase I/IIa trial that successfully demonstrated safety and immunogenicity of an FSP neoantigen-based vaccine in MSI colorectal cancer patients (Clinical trial number: NCT01461148). The vaccine was safe and induced robust cellular and humoral immune responses in all vaccinated patients. To further develop a cancer preventive vaccine against MSI cancers in Lynch syndrome, we aimed to establish a preclinical mouse model. A systematic database search was performed to identify cMS sequences in the murine genome. Subsequently, intestinal tumors obtained from Lynch syndrome mice (Msh2flox/flox VpC+/+) were evaluated for mutations affecting these candidate microsatellites. Thirteen candidate cMS were detected that presented with a mutation frequency of 15% or higher. Epitope prediction using the netMHC4.0 algorithm was performed, and ten most promising FSP neoantigens were synthesized. Immunogenicity was evaluated after vaccination of C57BL/6 mice using IFN-gamma ELISpot. Four FSP neoantigens derived from cMS mutations in the genes Nacad, Maz, Xirp1, and Senp6 elicited strong antigen-specific cellular immune responses. CD4-specific T cell responses were detected for Maz, Nacad, and Senp6 and CD8-positive T cells were detected for Xirp1 and Nacad. Vaccination with peptides encoding these four intestinal cancer FSP neoantigens promoted anti-neoantigen immunity, reduced intestinal tumorigenicity and prolonged overall survival (P&amp;lt;0.01). Additionally, NSAIDs, which have chemopreventive efficacy for Lynch syndrome, increase T cell immunity against neoantigens. Mechanistic tumor mutation burden and adaptive immune response studies will be shown. In summary, these data support the further development of vaccination strategies for preventing cancers associated with Lynch syndrome. Citation Format: Ozkan Gelincik, Hamza Ibrahim, Mine Ozkan, Aysel Ahadova, Shizuko Sei, Robert Shoemaker, Mattias Kloor, Magnus Von Knebel Doeberitz, Steven M. Lipkin. Frameshift neoantigen vaccination prevent Lynch syndrome mouse model intestinal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2732.
BACTERIAL VACCINE THERAPY: ITS INDICATIONS AND LIMITATIONS
Journal: JAMA (1913)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Billing Procedures for Laboratory Services
Journal: JAMA (1965)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The impact of human immunodeficiency virus infection in liver transplantation for hepatocellular carcinoma
Authors: Jean-Charles Duclos-Vallée, René Adam, Eric Vibert, Didier Samuel
Journal: Hepatology (2011)

We agree with these authors that one of the main problems concerning patients infected with human immunodeficiency virus (HIV)who have hepatocellular carcinoma (HCC) is the high rate of dropouts on the waiting list for liver transplantation (LT).1 Although controversial results have been published regarding the prognosis of HCC in HIV-infected patients, the kinetics of tumor progression in HIV-infected subjects seems to be particularly rapid.2, 3 We need specific markers of poor prognosis and HCC tumor progression in these patients in order to improve patient selection and guide neoadjuvant and adjuvant therapies. As for the CD4 cell count, we agree with the authors that great caution is necessary regarding the indications of LT in patients with a CD4 T cell count lower than 100/μL. However, because of the lack of clear data to demonstrate the influence of the CD4 T cell count on HCC progression before LT and on survival after LT, it is difficult to exclude such patients from a transplantation program. In the event of a low CD4 cell count before LT, one of the main objectives during the post-LT period is to prevent a marked drop in the CD4 cell count; for this reason, a rapid reintroduction of highly active antiretroviral therapy (HAART) after LT needs to be discussed in such cases. We also agree with the authors that mTOR (mammalian target of rapamycin) inhibitor-based immunosuppressive regimens must be tried in such patients.4 We contributed to the Silver study on sirolimus after LT for HCC, and rapamycin and sirolimus are currently being evaluated in our center for the treatment of HIV-infected patients who have undergone transplantation for HCC. However, mTOR inhibitors are metabolized by cytochrome P4503A4, and interactions with HAART therapy need to be avoided. Moreover, Raltegravir, an HIV-1 integrase inhibitor that is metabolized primarily by UGT1A1 (uridine diphosphate glucuronosyltransferase 1 family, polypeptide A1) and is not affected by cytochrome P450 inhibitors or inducers, could be suggested as the drug of choice among nucleoside reverse transcriptase inhibitors.5 In conclusion, the definition of new prognostic markers for HCC before LT, an active neoadjuvant therapy that can prevent dropouts, and the specific management of immunosuppression are the main objectives to be achieved in the very near future with respect to these HIV-infected patients. Jean-Charles Duclos-Vallée M.D.* , René Adam M.D., Ph.D.* § ¶, Eric Vibert M.D.* , Didier Samuel M.D.* , * Assistance Publique–Hôpitaux de Paris, Hôpital Paul Brousse, Centre Hepato-Biliaire, Villejuif, France, Institut National de la Santé et de Recherche Médicale (INSERM), Unité 785, Villejuif, France, Université Paris-Sud, Unité Mixte de Recherche (UMR)-S785, Villejuif, France, § INSERM, Unité 776, Villejuif, France, ¶ Université Paris-Sud, UMR-S776, Villejuif, France.
First-line pembrolizumab (P), trastuzumab (T), capecitabine (C) and oxaliplatin (O) in HER2-positive metastatic esophagogastric adenocarcinoma.
Authors: Yelena Yuriy Janjigian, Steven Brad Maron, Joanne F Chou, Amelia Gabler, Marc Simmons, Parisa Momtaz, Francisco Sanchez-Vega, Marina Shcherba, Geoffrey Yuyat Ku, Elizabeth Won, Curtis Robert Chong, Hans Gerdes, David Paul Kelsen, David H. Ilson, David B. Solit, Nikolaus Schultz, Pari M. Shah, Marinela Capanu, Jaclyn Frances Hechtman
Journal: Journal of Clinical Oncology (2019)

4011 Background: Trastuzumab stimulates HER2-specific T cell responses and increases tumor PD-L1 expression, and anti-PD-1 antibody can help enhance T cell-specific immunity of trastuzumab. We conducted a phase II trial of pembrolizumab with chemotherapy/trastuzumab. Methods: Patients (pts) with previously untreated HER2 IHC 3+ or FISH+ tumors irrespective of PD-L1 status received intravenous P 200 mg flat dose, T 6 mg/kg (after 8 mg/kg load), O 130 mg/m2 every 3 weeks and oral C 850 mg/m2 2 weeks on/1 week off. 22 pts received 1 cycle of induction P/T prior to initiation of chemotherapy. The primary endpoint was 6-months PFS; with target accrual of 37 pts. Secondary endpoints included safety, OS, ORR, and biomarker analysis. Results: Accrual completed and 100% of the 32 evaluable pts had tumor regression (ranging from -20% to -100%). The RECIST 1.1 ORR was 87% (25 PR, 3 CRs), and 12 (52%) of pts that received induction P/T x 1 cycle showed reduction in target lesions. Median PFS was 11.3 months (mo), with 67% 6 mo PFS. Median follow up was only 6.6 mo. In pts with available material, 14/36 (40%) had PD-L1 CPS &gt;1 and median TMB was 4.4 mut/Mb (0-10.6). There was no correlation between PD-L1 status and PFS or OS. ERBB2 amplification was evident by tissue-NGS in 17/29 (61%) and ctDNA-NGS in 17/30 (58%) pre-treatment, while the remaining pts were ERBB2- by NGS likely due to tumor heterogeneity or low tumor content. CtDNA maxVAF decreased in 16/24 tested pts after 1 cycle of induction T/P alone. irAEs included interstitial nephritis Gr4 (3%), transaminitis Gr3 (11%), Gr4 (3%), colitis Gr3 (3%). Conclusions: Most pts (51%) remain on therapy, and so the primary endpoint should be reached by 6/19. Updated survival, correlative studies and will be presented. These promising preliminary safety and efficacy results led to initiation of a definitive phase III Keynote 811 trial. Clinical trial information: NCT02954536.